Heart failure is commonly classified based on which heart function or which side of the heart is most affected. Left-sided heart failure describes a failure of the left-sided pumping action by which oxygen-rich blood from the lungs is moved through the left atrium into the left ventricle and then out into the rest of the body. The term right-sided heart failure is used for a failure of the right-sided pumping action which pumps blood that returns to the heart through the veins through the right atrium into the right ventricle and then back out into the lungs to have it replenished with oxygen. The symptoms of heart failure are further distinguished whether they have developed quickly (acute heart failure) or gradually over time (chronic heart failure). Congestive heart failure (CHF) describes the general condition in which the heart cannot pump enough blood to meet the needs of the body. As blood flow out of the heart slows, blood returning to the heart through the veins backs up, causing congestion in the tissues. Typical signs thereof are swollen legs or ankles, tiredness, difficulties of breathing, pulmonary edema, respiratory distress. CHF may be caused by coronary artery diseases, congenital and primary heart diseases, infections of the heart muscle (cardiomyopathy, endocarditis and/or myocarditis), myocardial infarctions, high blood pressure, heart valve diseases. CHF also affects the function of the kidneys. The drugs used in treatment of CHF are angiotensin inhibitors and vasodilators to expand blood vessels and decrease resistance, beta blockers to improve the function of the left ventricle, digitalis to increase the pumping action of the heart and diuretics for an elimination of excess salt and water.
The present disclosure relates to heart failures with preserved ejection fraction (HFPEF), also named heart failure with normal ejection fraction or simply diastolic heart failure (DHF), and more specifically to a HFPEF subgroup involving altered chemo-mechanical properties of the heart muscle proteins. Diastole is that phase of the cardiac cycle when the heart is not contracting to propel blood out (systole) to the body, brain and lungs but instead is relaxing and filling with incoming blood that is being returned from the body through the inferior vena cava (IVC) and through the superior vena cava (SVC). The HFPEF subgroup of heart failures is therefore associated with a decline in diastolic performance of the left ventricle of the heart. When the cardiac muscle has become stiff and lost its ability to relax the left ventricle is not readily filled with blood following contraction and the cardiac output becomes either diminished or an elevated ventricular diastolic pressure despite essentially normal end diastolic volume (EDV) is observed for compensation. The HFPEF is often characterized histologically by a hypertrophy of cardiomyocytes, increased interstitial collagen deposition and calcium deposition within the myocardium which are assumed to lead collectively to decreased distensibility and compliance. The chemo-mechanical characteristics of the heart muscle proteins as well as myocytes and the biophysics of the failing heart have not yet achieved clinical relevance.
There is no specific treatment of HFPEF available. When the chronic condition is tolerable by the patient, the therapy may be directed at aggravating factors such as high blood pressure and diabetes. Diuretics are often given. The administration of calcium channel and/or angiotensin II receptor blocker drugs may be of benefit in reducing ventricular stiffness in some cases but there is no favorable effect in mortality rates. A major complication is pulmonary edema the treatment of which by diuretics is often challenging since the stiffened heart and vessels of the patients are very susceptible to hypotensive events after salt and water excretion. Thus, there are no means and tools for treating persons afflicted of heart failure with preserved ejection fraction (HFPEF). The prior art therefore represents a problem.